What would be the effect on the cell cycle if a cell acquired a mutation that rendered each of the following domains inactive? Explain your reasoning. The PSTAIR region of an M-phase Cdk The Wee1 Kinase The kinase that normally phosphorylates Sic 1 The Sic1 cyclin-Cdk inhibitor
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What would be the effect on the cell cycle if a cell acquired a mutation that rendered each of the following domains inactive? Explain your reasoning.
- The PSTAIR region of an M-phase Cdk
- The Wee1 Kinase
- The kinase that normally phosphorylates Sic 1
- The Sic1 cyclin-Cdk inhibitor
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- You are studying three proteins that you think are important Yor progression through the cell cycle. You know that one of them is a phosphatase (P1) and the other two are kinases ( K1 and K2). You add these enzymes in different combinations as shown below, and find that they have different effects on the activity of a cyclin dependent kinase, cdk2p. cdk2p Inactive Active cdk2p + K1 cdk2p + K2 Inactive cdk2p + K1 + K2 Inactive cdk2p + P1 cdk2p + P1 + K2 cdk2p + P1 + K1 Inactive Inactive Active cdk2p + P1 + K1 + K2 ActiveDNA damage can suppress the activity of the following cyclin-dependent kinases EXCEPT G1/S-Cdk S-Cdk M-Cdk G1-Cdk Which phenomenon allows the formation of double and triple bonds between carbon atoms? * Reduction Radioactivity Oxidation Hybridization If an agent that disrupts microtubules activity was added to cells at M phase, the cells will ble expected to get arrested at Anaphase O Metaphase O Prophase Telophase O 0 OWhat is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.
- Which of the following small GTP-binding proteins does NOT play a role in cell migration during chemotaxis? O Cap Z Rho Cdc42 O All of the listed GTPases play a role in cell migration O Rac ◆ PreviousWhy doesn't Cdk1 active immediately upon binding to cyclin B? What other components of the cell’s regulatory machinery could explain the delay in activation of the kinase activity?# 3 You've engineered a mutant cell where the FADD adapter was truncated. The mutant FADD only contains the Death Domain, and lacks the Death Effector Domain. What is the most likely phenotypic outcome for this mutant cell when presented with the Fas ligand? 20 E O The Fas/FasL oligomer is formed, but apoptosis is blocked O The Fas/FasL oligomer is formed, and apoptosis is hyperactivated O The Fas/FasL oligomer is not formed, and apoptosis is blocked O The Fas/FasL oligomer is not formed, but apoptosis is hyperactivated F3 $ 4 DOD 000 R F4 % 5 F5 T BARAT 6 tv @ MacBook Air F6 Y & 7 F7 U * ➤11 8 F8 · 9 F9
- Rous Sarcoma Virus can cause cancer in infected cells. The tumor causing nature of the virus is linked to it harbouring a gene that codes for a unique receptor tyrasine kinase (RTK). What is it about the tyrosine kinase that accounts for the tumor-causing nature of the virus? O It is unrelated to any human kinase and thus is able to act uncontrollably in causing cell division. O It cantain activate downstream effectors without binding to a SH2 domain. O It lacks the carboxy-terminal regulatory domain that is present in RTKS of non-cancerous cells.What do you mean by S-phase cyclindependent kinases?Cyclin-dependent kinases are a type of "microchip" protein that require multiple inputs (i.e., structural alterations) to be activated-- and thus are active only under specific conditions (as shown in the diagram below). How does limiting activity to when all conditions have been met help the cell function properly? INPUTS has this phosphate been removed? been added? has this is cyclin present? phosphate
- What would most likely occur to nuclear-cytoplasmic shuttling if the intrinsic GTPase activity of RAN was slowed down by 50%? Group of answer choices RAN would not bind exportin and proteins would accumulate in the nucleus All of the answers are likely None of the answers are likely Importin beta would not release from RAN in the cytoplasm and nuclear import would slow down RAN would not bind to importin beta and protein cargo in the nucleus would not releaseThis phosphatase removes an inhibitory phosphotyrosine phosphate from serine protein kinase, mentioned in question 6, which activates kinase. What phosphatase is it? This is what question 6 says....This is the serine protein kinase that when activated in a complex cyclin, controls onset of mitosis and M-phase of the cell cycle. 1. Cyclin A/B 2. Wee 1 3. TOR (Target of Rapmycin) 4. Cdk1 5. none of the these ***I believe the answer is Cdk1 for number 6, but I could be wrongYou have discovered two new inhibitors that inhibit enzymes involved in the pathway shown below. Both inhibitors are newly identified proteins. You know that one of these proteins is a noncompetitive inhibitor of the G1/S-cyclin dependent kinase (G1/S-Cdk). Another protein is a competitive inhibitor of the phosphatase (ie. a regulatory enzyme) that removes phosphates from phosphorylated Rb. mitogen activated mitogen receptor intracellular signaling pathway activated G,-Cdk and G,/S-čdk inactivated Rb protein active Rb protein inactivated transcription regulator active transcription regulator PHOSPHORYLATION OF Rb TRANSCRIPTION TRANSLATION CELL PROLIFERATION 1. What effect would the noncompetitive inhibitor of the G1/S-Cdk complex have on the Rb protein in the pathway shown above? And what effect would that have on the final outcome for these cells? 2. What effect would the competitive inhibitor of the phosphatase that acts on phosphorylated Rb have on the final outcome for these cells?…
